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1.
Eur Arch Paediatr Dent ; 25(3): 327-334, 2024 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-38625491

RESUMEN

PURPOSE: To evaluate the proximal caries progression in primary molars using the radiographic International Caries Detection and Assessment System (ICDAS). METHODS: A study was conducted on 196 children aged 3-9 years old who underwent the clinical examination and bitewing radiography during baseline and 6-month (and over) follow-up visits. The primary molars bitewing radiographs with initial enamel caries (RA1 and RA2) or outer dentine caries (RA3) of proximal surfaces were included. Caries advancement was scored using ICDAS criteria and statistical analyses with the chi-square test. Median survival time was evaluated using Kaplan-Meier survival curves and log-rank tests. RESULTS: A total of 439 surfaces of primary molars were included in this study and an averaged follow-up period of enamel and dentine caries group were 18.3 ± 9.6 months and 16.5 ± 9.5 months respectively. The progression of proximal enamel lesions significantly differed between primary maxillary and mandibular molars (p = 0.002) and among each patient's primary mandibular second molar and the others (p = 0.002). On the contrary, the outer dentine caries of each group of primary molars was not different. The median survival time of the initial enamel proximal caries (23.30 months) was non-significantly longer than that of the dentine (20.80 months). CONCLUSIONS: Progressions of the initial enamel proximal caries were significantly different among primary molars at the average 18.3-month follow-up. The median survival period of the enamel proximal caries was more extended than that of dentine but without statistical difference. These results provide essential information for dentists regarding an appropriate appointment for bitewing examinations.


Asunto(s)
Caries Dental , Progresión de la Enfermedad , Diente Molar , Radiografía de Mordida Lateral , Diente Primario , Humanos , Caries Dental/diagnóstico por imagen , Diente Molar/diagnóstico por imagen , Diente Primario/diagnóstico por imagen , Niño , Preescolar , Estudios Retrospectivos , Masculino , Femenino , Esmalte Dental/diagnóstico por imagen , Esmalte Dental/patología , Dentina/diagnóstico por imagen , Dentina/patología , Estudios de Cohortes
2.
Clin Exp Immunol ; 167(1): 99-107, 2012 Jan.
Artículo en Inglés | MEDLINE | ID: mdl-22132889

RESUMEN

The non-catalytic region of tyrosine kinase (Nck) is proposed to play an essential role in T cell activation. However, evidence based on functional and biochemical studies has brought into question the critical function of Nck. Therefore, the aim of the present work was to investigate the role of Nck in T cell activation. To study this, the human Jurkat T cell line was used as a model for human T lymphocytes. The short interfering (si) RNA targeting Nck1 gene was used with electroporation to knock-down Nck1 protein expression in Jurkat T cells. Primary human CD4 T cells were also transfected with the siRNA of Nck1. The results showed that decreased Nck1 protein expression did not affect the apoptosis of the transfected Jurkat T cells compared with control siRNA-transfected cells and non-transfected cells. Upon CD3ε/CD28 stimulation, knock-down of Nck1 in Jurkat T cells caused a decrease in CD69 expression and in interleukin (IL)-2 secretion. Similarly, knock-down of Nck1 in primary CD4 T cells also caused decreased CD69 expression. However, no significant alterations of CD69 and IL-2 expression were found upon phytohaemagglutinin (PHA)/phorbol myristate acetate (PMA) stimulation. Knock-down of Nck1 had no effect on the proliferation of Jurkat T cells stimulated with either PHA or anti-T cell receptor (TCR) monoclonal antibody (C305). The reduced Nck1 expression in Jurkat cells was also associated with a reduced phosphorylation of extracellular regulated kinase (Erk)1 and Erk2 proteins upon CD3ε/CD28 stimulation. In conclusion, the decreased Nck1 protein in Jurkat T cells resulted in an impairment of TCR-CD3-mediated activation involving a defective Erk phosphorylation pathway.


Asunto(s)
Proteínas Adaptadoras Transductoras de Señales/fisiología , Linfocitos T CD4-Positivos/inmunología , Células Jurkat/inmunología , Proteína Quinasa 1 Activada por Mitógenos/metabolismo , Proteína Quinasa 3 Activada por Mitógenos/metabolismo , Proteínas Oncogénicas/fisiología , Complejo Receptor-CD3 del Antígeno de Linfocito T/inmunología , Inmunidad Adaptativa/inmunología , Proteínas Adaptadoras Transductoras de Señales/antagonistas & inhibidores , Proteínas Adaptadoras Transductoras de Señales/genética , Anticuerpos Monoclonales/inmunología , Anticuerpos Monoclonales/farmacología , Antígenos CD/biosíntesis , Antígenos CD/genética , Antígenos de Diferenciación de Linfocitos T/biosíntesis , Antígenos de Diferenciación de Linfocitos T/genética , Apoptosis/efectos de los fármacos , Apoptosis/inmunología , Antígenos CD28/inmunología , Linfocitos T CD4-Positivos/metabolismo , Electroporación , Humanos , Interleucina-1/biosíntesis , Interleucina-1/genética , Células Jurkat/efectos de los fármacos , Células Jurkat/metabolismo , Lectinas Tipo C/biosíntesis , Lectinas Tipo C/genética , Activación de Linfocitos/efectos de los fármacos , Activación de Linfocitos/inmunología , Proteínas Oncogénicas/antagonistas & inhibidores , Proteínas Oncogénicas/genética , Fosforilación , Fitohemaglutininas/farmacología , Procesamiento Proteico-Postraduccional , Interferencia de ARN , ARN Interferente Pequeño/farmacología , Acetato de Tetradecanoilforbol/farmacología
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